Abstract

Viruses hijack host functions to invade their target cells and spread to new cells. Specifically, viruses learned to usurp liquid‒liquid phase separation (LLPS), a newly exploited mechanism, used by the cell to concentrate enzymes to accelerate and confine a wide variety of cellular processes. LLPS gives rise to actual membraneless organelles (MLOs), which do not only increase reaction rates but also act as a filter to select molecules to be retained or to be excluded from the liquid droplet. This is exactly what seems to happen with the condensation of SARS-CoV-2 nucleocapsid protein to favor the packaging of intact viral genomes, excluding viral subgenomic or host cellular RNAs. Another older pandemic virus, HIV-1, also takes advantage of LLPS in the host cell during the viral cycle. Recent discoveries highlighted that HIV-1 RNA genome condensates in nuclear MLOs accompanied by specific host and viral proteins, breaking the dogma of retroviruses that limited viral synthesis exclusively to the cytoplasmic compartment. Intriguing fundamental properties of viral/host LLPS remain still unclear. Future studies will contribute to deeply understanding the role of pathogen-induced MLOs in the epidemic invasion of pandemic viruses.

中文翻译：

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由大流行病毒重组和构建的无膜细胞器：HIV-1和SARS-CoV-2

摘要

病毒劫持宿主功能以侵入目标细胞并传播到新细胞。具体来说，病毒学会了篡夺液液相分离（LLPS），这是一种新开发的机制，细胞利用该机制来浓缩酶，以加速和限制各种细胞过程。LLPS 产生了真正的无膜细胞器 (MLO)，它不仅提高了反应速率，而且还充当过滤器来选择要保留或从液滴中排除的分子。这正是 SARS-CoV-2 核衣壳蛋白浓缩时发生的情况，有利于完整病毒基因组的包装，不包括病毒亚基因组或宿主细胞 RNA。另一种较古老的大流行病毒 HIV-1 在病毒周期中也利用了宿主细胞中的 LLPS。最近的发现强调，HIV-1 RNA 基因组在核 MLO 中凝结，并伴有特定的宿主和病毒蛋白，打破了逆转录病毒将病毒合成仅限制在细胞质区室的教条。病毒/宿主 LLPS 的有趣基本特性仍不清楚。未来的研究将有助于深入了解病原体诱导的 MLO 在大流行性病毒的流行性入侵中的作用。